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J Cell Mol Med. 2019 Nov 12. doi: 10.1111/jcmm.14808. [Epub ahead of print]

The expression of miR-125b in Nrf2-silenced A549 cells exposed to hyperoxia and its relationship with apoptosis.

Author information

1
Department of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.

Abstract

Bronchopulmonary dysplasia (BPD) is a chronic lung disease that affects the quality of life of infants. At present, premature exposure to hyperoxia for extended periods of time is believed to affect the development of lung tissue and vascularity, resulting in BPD. The oxidative stress caused by hyperoxia exposure is an important risk factor for BPD in premature infants. Nuclear factor E2-related factor 2 (Nrf2) is an important regulator of antioxidant mechanisms. As a microRNA, microRNA-125b (miR-125b) plays an important role in cell proliferation, differentiation and apoptosis. Although the Nrf2/ARE pathway has been extensively studied, little is known about the regulatory role of microRNAs in Nrf2 expression. In this study, the expression levels of Nrf2 and miR-125b in the lung tissues of premature Sprague Dawley (SD) rats and A549 cells exposed to hyperoxia were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and the apoptosis of A549 cells was detected by flow cytometry. The results showed that Nrf2 and miRNA-125b in the lung tissues of premature rats increased significantly upon exposure to hyperoxia and played a protective role. Nrf2 was suppressed by small interfering RNA (siRNA) in A549 cells, miR-125b was similarly inhibited, and apoptosis was significantly increased. These results suggest that miR-125b helps protect against BPD as a downstream target of Nrf2.

KEYWORDS:

Nrf2; bronchopulmonary dysplasia; miR-125b; premature; siRNA

PMID:
31713992
DOI:
10.1111/jcmm.14808
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